FATAL INTRACEREBRAL HAEMORRHAGE WITH ACUTE RENAL FAILURE WITHOUT ANY LOCAL MANIFESTATION : A RARE SEQUELAE FOLLOWING SNAKE BITE

Dr. Abhijeet Singh Sachan, Dr. Prakrati Sachan, Dr. Surjeet Singh and Dr. Sateesh Chandra Verma ...................................................................................................................... Manuscript Info Abstract ......................... ........................................................................ Manuscript History Received: 10 May 2020 Final Accepted: 15 June 2020 Published: July 2020

Snake bite is common entity in tropical countries . India has maximum no of snake bite related deaths . The deaths are commonly due to haemotoxic and neurotoxic properties of snake venom . Intracranial findings occur with activation of coagulation pathway by procoagulant toxins. The snake venom has some toxins and enzymes namely proteases ,prothrombinase,metalloproteinases ,collagenase ,haemorrhagins . Cerebral haemorrhage include intraparenchymal , intraventricular , subarachnoid bleed . Acute tubular necrosis is the most common renal manifestation . These patients are usually treated with polyvalent antisnake venom . They have poor prognosis once cerebral manifestations occur .

Introduction:-
Snake bite is a common cause of death in certain parts of the world. India leads the world with maximum number of snakebites and related mortality globally . 1 Approximately 4-18 million people have snakebite worldwide and 20,000 -94,000 people die every year . 2 In India annually approximately 2,500,000 snakebites are reported with 30,000-50,000 deaths per year. 3 Deaths can be attributed to there haematotoxic and neurotoxic properties . Elapids (Cobra , Mamba, and Coral snakes and Kraits ) are neurotoxic whereas Vipers( Russells viper,pit viper ,rattle snake ) Tiger snake , Twig snake are haemotoxic .Clinical presentation of neurotoxicity include hypotension ,shock, multiorgan failure while haemotoxicity manifest in the form of local tissue swelling ,necrosis ,bleeding and coagulopathy. [4][5][6] Cerebral complication include both haemorrhagic and non-haemorrhagic manifestations . Cerebral haemorrhage include intraparenchymal , intraventricular , subarachnoid bleed .The mechanism is believed to cause toxin induced coagulopathy . This case had all the cranial manifestation without any local symptom .

Case Report:
A 60 year old nondiabetic and non-hypertensive female patient presented with history of snakebite 4 days back . She ignored this incident and fell unconscious 3 days after the incident, with no preceding vomiting and headache . She was brought to our centre with GCS of 7/15 , and laboured breathing . Her pupils were equal and sluggishly reactive to light .Her blood pressure was 114/72 mmHg , pulse rate was 96/min and respiratory rate was 20 /min . There was a snakebite mark seen on Right toe .There was no signs of head injury , any external bleeding ,local ecchymosis, local tissue necrosis , DVT . She was immediately intubated and NCCT Head was done which showed a large intraparenchymal haemorrhage in right occipital with intraventricular extension and subarachnoid haemorrhage ( Figure 1 ) .With persistent clinical deterioration she was put on ventilatory support .Gradually she developed haematuria and acute renal failure .
Corresponding Author:-Dr. Abhijeet Singh Sachan  (Table 1) .Her USG abdomen was done which showed maintained corticomedullary junction in bilateral kidney . Treatment : She was initially managed with antisnake venom therapy with 10 vials -100 ml in 500 ml of .9% saline over 2 hours . After that fresh frozen plasma and platelet concentrates were administered to correct coagulation profile . She was managed conservatively with supportive treatment with broad spectrum antibiotics , antiepileptic ( phenytoin) , mannitol and ventilator support .With gradual deterioration of neurological status , vasopressor therapy was started . The patient did not show any improvement and finally succumbed to death after 4 days .

Discussion:-
Snake bite is a common cause of mortality and morbidity in the world with common incidence in Africa , South America and South East Asia . In India Maharashtra has the maximum incidence ( 70 per lakh population ). Mosquera et al reported a 2.6% incidence of cerebrovascular complication among 309 patients with 7 cases of cerebral haemorrhage . 7 Common Kraits and vipers are responsible for most of the snakebites in india .
Clinically they present with symptoms of neurotoxicity ,haemorrhagic manifestations ,systemic vasculotoxicity , local complications and renal failure .Cerebral involvement after snake bite is rare and includes both infarcts and haemorrhages . Cerebral haemorrhages following snakebite occur mostly due to two phenomenons i) venom induced coagulopathy ii) Haemorrhage induced direct endothelial damage . 8 The snake venom has some toxins and enzymes namely proteases , prothrombinase,metalloproteinases ,collagenase ,haemorrhagins ,thrombin like enzymes , polypeptide toxin ( cardiotoxin,bradykinin and histamine ) and toxic acidic proteins .These products interfere with normal clotting mechanism by producing anticoagulant and coagulant impacts .The viper venom also contain various anticoagulant proteins and activate factors V ,IX,X, XIII causing fibrinolysis and haemorrhage . 9 VICC (Venom induced consumption coagulopathy) occurs as result of activation of coagulation pathway by procoagulant toxins .It is characterized by prolonged 20WBCT ,PT,PTTK and fibrin degradation products . 10 On the other hand Metalloproteins (ecarin and carinactivase ) are prothrombin activators which reduce the level of fibrinogen , factor V, and factor VII resulting in cerebral haemorrhage . 11 ,12,13 Proteases activate fibrinolysis and cause destruction of blood vessels and results in Cerebral haemorrhages . 14 Haemorrhagin toxin can lead to both VICC and direct endothelial damage and can result in cerebral haemorrhages including subarachnoid haemorrhage . 10 Toxic acidic proteins Parenchymal brain hemorrhages Acute renal failure is a common complication .Its prevalence ranges from 2-10% . 15 The most common finding is acute tubular necrosis but renal cortical necrosis can be seen . 16 .The probable mechanism is suggested to be fibrin microthrombi deposition at the glomerular capillary tuff , myoglobinuria and direct injury due to toxins . 17,18 The mainstay of treatment of snake bite is Anti Snake Venom .The vaccine is polyvalent and effective against all the four common species ; Russells viper , common cobra ,common krait and saw scaled viper . Approx 1 mL of antisnake venom neutralizes 0.60 mg of cobra venom, 0.45 mg of krait venom, 0.6 mg of Russell viper venom, and 0.45 mg of saw-scaled viper venom .Begin with 10 vials of ASV in 100 ml of saline for 2 hours . The dose needs to be repeated after 6 hours , if 20 WBCT is derranged .

Conclusion:-
Intracerebral event after snake bite is a rare complication involving infarct and haemorrhage .It is associated with poor prognosis and should be managed promptly with Antisnake venom and correction of coagulation profile with Fresh frozen plasma for better outcome .Intracerebral haemorrhagic complications often result in increased intracranial pressure and brainstem herniation . A comprehensive measure should be taken for to improve the outcome after snake bite .